Heart Failure

Heart Failure

1. Intro

   • Common
     • 1-3% general population & 10% of elderly people
   • Prognosis
     • Poor; 25-40% 5Y mortality
       • Higher BNP = higher CV and all-cause mortality. A/w sudden death.
         • Persistent increased BNP despite vigorous Rx predicts adverse outcomes
   • Definition
     • Clinical syndrome that is characterised by inability of heart to maintain a CO that is sufficient for the body's needs

2. Classification and corresponding causes

   • Low output most common = low CO that fails to increase w/ exertion
     • Pump failure
       • Systolic dysfunction - <40% EF
         • MI, IHD, CM
       • Diastolic dysfunction - EF >50%
         • Constrictive pericarditis, restrictive CM, tamponade, HTN
       • Decreased HR
         • BB, MI, heart block
       • -vely inotropic drugs eg antiarrhythmics
     • Excessive preload
       • AR, MS, MR or fluid overload
         • More likely if renal impairment, or big volumes involved, or simultaneous cardiac insult, or elderly
     • Excessive afterload
       • AS, HTN
     • NYHA classification of sx severity
   • high output = CO high/normal but incr needs
     • Anaemia, pregnancy, paget's, hyperthyroidism, AVMs, beri beri

3. Investigations and diagnosis

   • If normal ECG and BNP then diagnosis unlikely
     • If either AN then echo required
       • Can indicate a cause ± presence of LV dysfunction
     • >100 then +ve, if <50 then -ve
       • Highest in those w/ syst + diastolic dysfunction.
   • Sx of HF and objective evidence of dysfunction at rest.
     • Framingham criteria for CCF
       • 2 majors or 1 major and 2 minors
         • Major
           • PND, creps, S3 gallop, cardiomegaly, increased CVP (>16cmH20 in RA), >4.5kg w loss in 5/7 of treatment, Neck vein distension, acute pulmonary oedema, hepatojugular reflux
         • Minor
           • Bilateral ankle oedema, dyspnoea on ordinary exertion, tachycardia (>120), dec vital capacity by 1/3, nocturnal cough, hepatomegaly, pleural effusion.
     • Other signs of HF
       • Exhaustion, cool peripheries, cyanosis, low BP, narrow pulse pressure, pulsus alternans, displaced apex (LV dilatation), RV heave (pulmonary htn), murmurs of aortic or mitral valve disease, wheeze
   • Routine Ix
     • Bloods - FBC, U&E's, BNP
     • CXR - classical features
     • ECG - may indicate a cause eg LVH, MI, ischaemia. Rarely normal ECG in chronic HF.

4. Management

   • Acute - emergency mx
     • ABC mx
       • Airway - 100% oxygen unless COPD
         • Breathing - ABG, CXR
           • Circulation - IV access, ECG, Temp, UO. Start IV diamorphine 2.5-5mg slowly (caution if liver disease or COPD).
             • Furosemide 40-80mg IV slowly, more if renal failure too.
               • If SBP >90mmHg then GTN SL, if SBP ≥100 and still breathless start ISDN infusion, keeping SBP > 90.
   • Chronic mx
     • Conservative
       • Stop smoking, reduce salt, weight loss, nutrition etc
       • MDT
         • HF nurses, chest physio, OT
     • Medical
       • Treat any underlying causes, treat exacerbating factors eg thyroid disease, anaemia, infection, HTN
       • Drugs that improve prognosis
         • Diuretics
           • Loops reduce sx eg furos 40mg/day or bumet 1-2mg/day. SE = low K, renal impairment (requires large doses). ? thiazide if refractory oedema eg metolazone 5-20mg/day
             • Add K sparing if K<3.2, predisposed to arrhythmia, concurrent digoxin therapy (hypoK increases risk of dix toxicity), K losing condition.
         • ACEI
           • Dec mortality in proportion to LV dysfunction, dec risk of hospitalisation, provide sx relief in 1/52 approx.
             • AKI, K imbalances, cough, 1st dose hypotension, angiooedema (non-allergic)
         • B blockers
           • Start after ACEI and diuretic, start low and slow.
             • Cold peripheries, sleep disturbance, fatigue, impotence and loss of libido, loss of warning signs of hypoglycaemia can be lost
         • Sprinolactone (both)
           • In patients that are still sx despite other max therapy, prevents remodelling, and improves endothelial function. Little risk of hyperK even if taking ACEI.
         • Vasodilators (equal)
           • Hydralazine (DI lupus) + ISDN if intolerant to ACEI and ARBs. Reduces mortality in black people with HF, in combo w/ standard therapy.
       • Drugs for sx relief only
         • Digoxin
           • Helps even in SR. ? if LV systolic dysfunction + signs and sx of HF despite standard therapy inc ACEI and BB. Or ? in AF.
             • Maintain K 4-5. HypoK increases risk of toxicity.
               • Sx of toxicity
                 • Dec cognition, yellow/green halos, arrhythmias, N, anorexia.
               • If serious arrhythmia, correct hypokalaemia, and give Digibind - dig specific ab fragments taken from immunised sheep.
         • Diuretics
     • Surgical
       • ICD
       • Transplant

5. Mechanism of disease

   • Compensatory mechanisms that try to maintain perfusion and CO when the heart begins to fail.
     • These become pathological as the failure progresses
     • SNS activation
       • Increased preload through venoconstriction. But increased after load due to arteriolar constriction.
     • RAAS activation
       • Increased fluid retention, with increased after load due to AII.
     • Natriuretic peptides
       • Released by atria, ventricles, and vasc endothelium
         • Water, salt loss, relaxes smooth muscle (dec preload). ?Compensatory mechanism but inadequate.
           • Sensitivity >90%, specificity 80-90%
             • Not raised in acute HF exacerbation. Low if no LV dysfunction or HF.
         • Secretion inc by glucocorticoids, tachycardia, thyroid hormones. Endothelin1 and AII influence secretion.
     • LV dilatation
       • Decreased ejection of blood - stretched ventricle. Over time starling response flattened and increased venous pressure.
     • Hypertrophy, loss of myocytes and increased fibrosis leading to irreversible pump failure.